Acute myocardial infarction (AMI) is one of the leading causes of death in the Western world and many risk factors, both environmental and genetic, contribute to its pathogenesis. The heart generally lacks an endogenous regenerative capacity sufficient for repair after injury. Consequential left ventricular (LV) remodeling after myocardial infarction (MI) or other ischemic events leads to LV dilatation and ultimately to heart failure (Holmes et al., 2005, Annu Rev Biomed Eng.; 7:223-53). Immediately after coronary occlusion, ischemic myocytes downstream from the occlusion become necrotic and/or undergo apoptosis. Neutrophils infiltrate the tissue immediately, while leukocytes, predominantly macrophages, arrive shortly thereafter and participate in digestion of necrotic cellular debris. Neutrophils in the ischemic tissue can be toxic to the surrounding myocytes, because they release reactive oxygen species and proteolytic enzymes which further injure the surrounding myocytes (Nah & Rhee, Korean Circ J.; October; 39(10):393-82009). Once damage occurs, a hypocellular scar forms that leads to contractile dysfunction and eventual heart failure.
To reduce the epidemiologic and fiscal burden associated with ischemic events affecting the myocardium, it is imperative that new compositions and strategies be developed to preserve cardiomyocyte survival or stimulate cardiomyocyte growth following injury caused by ischemic events such as myocardial infarction. There is a need for therapies that can address and/or treat cardiac (e.g., myocardial) tissue following an injury. The invention disclosed herein addresses these needs and provides additional benefits as well.